Progression of liver disease is dependent on intercellular signaling, including those mediated by extracellular vesicles (EVs). Within these EVs, microRNAs (miRNAs) are packaged to selectively silence gene expression in recipient cells for upregulating or downregulating a specific pathway. Injured hepatocytes secrete EV-associated miRNAs which can be taken up by liver sinusoidal endothelial cells, immune cells, hepatic stellate cells, and other cell types. In addition, these recipient cells will secrete their own EV-associated miRNAs to propagate a response throughout the tissue and the circulation. In this review, we comment on the implications of EV-miRNAs in the progression of alcohol-associated liver disease, metabolic dysfunction-associated steatohepatitis, viral and parasitic infections, liver fibrosis, and liver malignancies. We summarize how circulating miRNAs can be used as biomarkers and the potential of utilizing EVs and miRNAs as therapeutic methods to treat liver disease.
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http://dx.doi.org/10.1055/a-2494-2233 | DOI Listing |
Ann Intern Med
January 2025
Department of Medicine, Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts (S.M.J.A., M.L.).
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease in the United States. It is characterized by steatosis in the liver and is potentially reversible. Risk factors include obesity, type 2 mellitus, and other metabolic disorders.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Internal and Experimental Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Important health disparities are observed in the prevalence of obesity and associated non-communicable diseases (NCDs), including type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD) among ethnic groups. Yet, the underlying factors accounting for these disparities remain poorly understood. Fructose has been widely proposed as a potential mediator of these NCDs, given that hepatic fructose catabolism can result in deleterious metabolic effects, including insulin resistance and hepatic steatosis.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Gastroenterology and Hepatology and Laboratory of Gastrointestinal Cancer and Liver Disease, West China Hospital, Sichuan University, Chengdu, 610041, China.
Skeletal muscle atrophy (sarcopenia) is a serious complication of liver cirrhosis, and chronic muscle inflammation plays a pivotal role in its pathologenesis. However, the detailed mechanism through which injured liver tissues mediate skeletal muscle inflammatory injury remains elusive. Here, it is reported that injured hepatocytes might secrete mtDNA-enriched extracellular vesicles (EVs) to trigger skeletal muscle inflammation by activating the cGAS-STING pathway.
View Article and Find Full Text PDFJ Int Med Res
January 2025
Divisions of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada.
Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the gene, potentially disrupting lipid metabolism and leading to dyslipidemia (DLD) and steatotic liver disease (SLD). Although SLD has been described in RTT mouse models, it remains undocumented in humans. We herein describe a 24-year-old woman with RTT who was evaluated for abnormal liver enzymes.
View Article and Find Full Text PDFPLoS One
January 2025
Division of Gastroenterology and Hepatology, University of Iowa, Iowa City, IA, United States of America.
Background: The July effect in US teaching hospitals has been studied with conflicting results. We aimed to evaluate the effect of physician turnover in July on the clinical outcomes of patients hospitalized with cirrhosis.
Methods: We utilized the Nationwide Inpatient Sample database (2016-2019) to identify patients hospitalized with cirrhosis and liver-related complications (variceal bleeding, hepatorenal syndrome, acute-on-chronic liver failure).
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